Spontaneous coronary artery dissection is a rare cause of acute coronary syndrome. Recurrent spontaneous dissection is even more rare. A case of recurrent coronary artery dissection is reported and the literature is reviewed.

RationaleA high cytosolic Na + concentration ([Na + i]) impairs contractility of myocardium from patients with advanced heart failure (HF) and since the Na + -K + pump maintains a low [Na + i], targeting pump function might be beneficial. Objective Determine if cardiac myocyte Na + -K + pump function is impaired in rabbits with severe congestive HF and whether in vivo treatment with β3 adrenoceptor (β3 AR) agonists, that are known to stimulate the pump in vitro, reverses the HF syndrome. Assess the clinical response when patients with advanced treatment-resistant HF are prescribed a β3 AR agonist. Methods and ResultsCoronary ligation caused marked organ congestion and ascites in rabbits. Na + -K + pump current of myocytes from non-infarcted myocardium was decreased. This was reversed by β3 AR agonist treatment that also significantly reduced organ congestion and prevalence of ascites. Animal models cannot examine if efficacy is additive to guideline-directed drugs up-titrated to maximal tolerated doses. We studied outcomes of 9 patients hospitalized with advanced HF (stage D) refractory to maximally tolerated treatment as assessed by ≥ 2 cardiologists. One-year mortality of such patients is 75% with medical treatment and almost all die within 2 years, 90% from HF. The off-label oral treatment with the β3 AR agonist mirabegron rapidly improved signs and symptoms on a time scale similar to that of the rabbits. Improvement of ≥1 NYHA Class was maintained early post-discharge with continued treatment. One patient died from HF at 16 months, 4 died from other causes at 2 -30 months and 4 remain alive at 32 ± 5 months with NYHA Class II symptoms. ConclusionsParallel treatment-induced reversal of Na + -K + pump inhibition and features of HF in rabbits provides mechanistic rationale for efficacy of β3 AR agonists. Improved in-hospital clinical trajectory and more favourable post-discharge course than expected suggest efficacy of mirabegron in advanced human HF.